中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (7): 1196-1201.doi: 10.4103/1673-5374.251290

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

Toll样受体4和蛋白酶激活受体2在神经系统的生理学和病理生理学方面:不仅仅是受体合作?

  

  • 出版日期:2019-07-15 发布日期:2019-07-15

Toll-like receptor 4 and protease-activated receptor 2 in physiology and pathophysiology of the nervous system: more than just receptor cooperation?

Darius Widera 1 , Rocío Martínez Aguilar 1, 2 , Graeme S. Cottrell 3   

  1. 1 Stem Cell Biology and Regenerative Medicine Group, School of Pharmacy, University of Reading, Whiteknights campus, Reading, UK
    2 Unidad de Inmunología, IBIMER, Universidad de Granada, Granada, Spain
    3 Cellular and Molecular Neuroscience, School of Pharmacy, University of Reading, Reading, UK
  • Online:2019-07-15 Published:2019-07-15
  • Contact: Darius Widera, PhD, d.widera@reading.ac.uk.

摘要:

orcid: 0000-0003-1686-130X (Darius Widera)
           0000-0001-9098-7627 (Graeme S. Cottrell)

Abstract:

Toll-like receptor 4 (TLR4) and protease-activated receptor 2 (PAR2) play pivotal roles in the mammalian innate immune response. Notably, in addition to their involvement in detection of invading pathogens, PAR2 and TLR4 modulate the levels of cell death-induced sterile inflammation by activating pro- or anti-inflammatory downstream signaling cascades. Within the central nervous system, there is emerging evidence that both receptors are involved in synaptic transmission and brain plasticity. Furthermore, due to their prominent role in mediating neuroinflammation, PAR2 and TLR4 are associated with development and progression of neurodegenerative disorders including but not limited to Alzheimer’s disease, Parkinson’s disease and multiple sclerosis. In this article, we summarise the current knowledge on the cooperation between PAR2 and TLR4, discuss the potential cross-talk levels and highlight the impact of the cross-coupling on neuroinflammation.

Key words: signaling, inflammation, proteases, myeloid of differentiation primary response gene 88, TIR-domain containing adaptor inducing interferon, lipopolysaccharide, TLR4, PAR2